AUTHOR=Ma Zejun , Zhu Lili , Liu Yan , Wang Zhida , Yang Yang , Chen Liming , Lu Qiulun 

TITLE=Lovastatin Alleviates Endothelial-to-Mesenchymal Transition in Glomeruli via Suppression of Oxidative Stress and TGF-β1 Signaling

JOURNAL=Frontiers in Pharmacology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2017.00473

DOI=10.3389/fphar.2017.00473

ISSN=1663-9812

ABSTRACT=<p>Statins may decrease chronic kidney diseases (CKDs) risk, but their underlying molecular mechanisms are not completely understood. Recent studies indicate Endothelial-to-mesenchymal transition (EndMT) plays an important role contributing to renal interstitial fibrosis. In the present study, we first investigated whether lovastatin could ameliorate renal fibrosis via suppression of EndMT and its possible mechanism. <italic>In vitro</italic> experiments, lovastatin significantly ameliorated microalbuminuria and pathologic changes in diabetic rats. Double labeling immunofluorescence showed lovastatin could inhibit EndMT in glomeruli. Furthermore, lovastatin could inhibit oxidative stress and down-regulate TGF-β1-Smad signaling. Consistent alterations were observed <italic>in vivo</italic> that lovastatin substantially suppressed EndMT and TGF-β1 signaling induced by high glucose in glomerular endothelial cells (GEnCs). These data indicated that lovastatin could ameliorate EndMT in glomeruli in diabetic nephropathy, the mechanism of which might be at least partly through suppression of oxidative stress and TGF-β1/Smad signaling pathway.</p>